When eggs and sperm form, chromosomes swap stretches of DNA in events called crossovers, a reshuffling essential both to genetic diversity and to chromosomes separating correctly. For decades the leading explanation for why males and females differ in crossover rates came down to chromosome structure: longer chromosome axes, more crossovers. A Cornell-led study in Molecular Biology and Evolution now shows that model is incomplete.
Analysing five genetically diverse mouse strains and tracking multiple stages of recombination, researchers in Paula Cohen's laboratory at the College of Veterinary Medicine, led by research associate Tegan Horan, found cases that defy the structural rule. In the PWD strain, males produced more crossovers than females despite shorter chromosome structures. The sexes differed in how efficiently they converted early DNA repair events into mature crossovers, and in the molecular pathways regulating where crossovers land.
The team also characterised a relatively rare class of crossovers that, despite being a small fraction of the total, guarantees each chromosome pair receives at least one, guarding against segregation errors. The stakes are considerable: studies estimate that 30 to 70 per cent of human eggs carry the wrong number of chromosomes, a leading cause of infertility, miscarriage and conditions such as Down syndrome. The authors conclude that meiosis follows no single universal blueprint.